Evidence map›Paper›PMID 42589121›Full record

ReviewBiology2026

Dynamic Cellular Regulation of Proteasome Translocation and Phase Transition.

Conner Butcher, Jianhui Li

Abstract readReview
In one paragraph

Review in Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Conner ButcherDepartment of Biomedical Engineering and Science, Florida Institute of Technology, Melbourne, FL 32901, USA.ORCID 0009-0003-8949-3664
Jianhui LiDepartment of Biomedical Engineering and Science, Florida Institute of Technology, Melbourne, FL 32901, USA.ORCID 0000-0001-8809-845X

Funding

Florida Department of Health 26C18
6 · The paper itself

Abstract

Proteasome dysfunction has been implicated in the pathogenesis of many human diseases, and the proteasome system has emerged as a major therapeutic target for cancer treatment. Besides proteasome activity, the dynamics of proteasome localization provide another tier of mechanism for regulating proteasome function and cellular protein homeostasis. While proteasomes are highly enriched in the nucleus, they can dynamically reshuffle across cellular compartments in response to metabolic cues. This localization shift is coupled with autophagy as a major mechanism for cell survival under stress. Under certain metabolic stress, proteasomes can reorganize into distinct membraneless condensates, termed proteasome condensates. While the current understanding of the biological significance of proteasome condensates is limited, they may provide proteolytic control to meet metabolic needs under stress. This review highlights how distinct metabolic cues, such as carbon starvation, amino acid deficiency, and senescence, regulate divergent proteasome fates including proteasome subcellular translocation, autophagic degradation of proteasomes, and proteasome condensate formation. A better understanding of proteasome regulation in a spatiotemporal manner will help identify new therapeutic targets for diseases affected by proteasome dysfunction.

Indexed as

autophagyliquid–liquid phase separationmetabolic stressnucleocytoplasmic translocationproteasome condensatesproteasome translocation dynamicsproteostasisubiquitin–proteasome system

Identifiers

PMID42589121
PMCPMC13465156

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.